OBJECTIVETo detect the expression of miRNA in de novo and complete response SAA patients and predict the targets of the miRNAs.

METHODSThe expression profiles of miRNA from bone marrow mononuclear cells of the SAA patients with de novo and CR were detected by miRNA microarray.

RESULTSTotally 35 up-regulated and 37 down-regulated miRNA were identified in CR SAA patients in comparison with de novo SAA patients. Furthermore, by predicting the targets of the differentlly expressed miRNA, it was found that some targets associated with T cell receptor signaling pathway and cell adhesion molecules.

CONCLUSIONSome miRNA may be involved in the pathogenesis of SAA.

BACKGROUNDPatients with premature triple-vessel disease (PTVD) have a higher risk of recurrent coronary events and repeat revascularization; however, the long-term outcome of coronary artery bypass grafting (CABG), percutaneous coronary intervention (PCI), and medical therapy (MT) alone for PTVD patients is controversial. The aim of this study is to evaluate the long-term outcome of PTVD patients among these three treatment strategies, to find out the most appropriate treatment methods for these patients.

METHODSOne thousand seven hundred and ninety-two patients with PTVD (age: men ≤50 years and women ≤60 years) were enrolled between 2004 and 2011. The primary end point was all-cause death. The secondary end points were cardiac death, myocardial infarction, stroke, or repeat revascularization.

RESULTSPCI, CABG, and MT alone were performed in 933 (52.1%), 459 (25.6%), and 400 (22.3%) patients. Both PCI and CABG were associated with lower all-cause death (4.6% vs. 4.1% vs. 15.5%, respectively, P < 0.01) and cardiac death (2.8% vs. 2.0% vs. 9.8%, respectively, P < 0.01) versus MT alone. The rate of repeat revascularization in the CABG group was significantly lower than those in the PCI and MT groups. After adjusting for baseline factors, PCI and CABG were still associated with similar lower risk of all-cause death and cardiac death versus MT alone (all-cause death: hazard ratio [HR]: 0.35, 95% confidence interval [CI]: 0.23-0.53, P < 0.01 and HR: 0.35, 95% CI: 0.18-0.70, P = 0.003, respectively, and cardiac death: HR: 0.32, 95% CI: 0.19-0.54, P < 0.01 and HR: 0.36, 95% CI: 0.14-0.93, P = 0.03, respectively).

CONCLUSIONSPCI and CABG provided equal long-term benefits for all-cause death and cardiac death for PTVD patients. Patients undergoing MT alone had the worst long-term clinical outcomes.

TRIAL REGISTRATIONClinicalTrials.gov; Identifier: NCT02634086. https://www.clinicaltrials.gov/ct2/show/record/NCT02634086?term=NCT02634086&rank=1.

OBJECTIVETo observe the effect of admission blood urea and creatinine levels on mortality in elderly patients with hip fracture.

METHODSForm January 2013 to December 2014, 767 elder patients with hip fracture were treated in our hospital including 253 males and 514 females, aged from 65 to 96 years old with an average of(75.67±6.81) years old. According blood urea and creatinine levels, the 767 hip fracture patients were divided into four groups as follow: group A(blood urea>=5 mmol/L, creatinine>=70 μmol/L); group B (blood urea>=5 mmol/L, creatinine<70 μmol/L); group C (blood urea<5 mmol/L, creatinine>=70 μmol/L); group D(blood urea<5 mmol/L, creatinine<70 μmol/L). In group A, there were 211 patients including 70 males and 141 females, aged from 65 to 95 years old with an average of(80.24±6.51) years old; in group B, there were 355 patients including 125 males and 230 females, aged from 65 to 93 years old with an average of(78.46±7.09) years old; in group C, there were 36 patients including 11 males and 25 females, aged from 65 to 95 years old with an average of (77.83±6.78) years old; in group D, there were 165 patients including 47 males and 118 females, aged from 65 to 96 years old with an average of (76.71±8.35) years old. The survivals and dead patients in four groups were collected and in-hospital mortality rate, 3-month, 12-month and 18-month mortality rate of patients were calculated. COX regression analysis was performed on these data, and clinical significance of serum urea and creatinine at admission in the elderly patients was researched.

RESULTSAll 767 hip fracture patients were followed up from 18 to 24 months with an average of (21.33±1.25) months, 159 patients were died in follow up period. The in-hospital mortality rate in 3-month, 12-month and 18-month mortality rate of the patients with high blood urea and high blood creatinine (urea>=5 mmol/L, creatinine>=70 μmol/L) were 2.37%, 9.95%, 16.11% and 26.07%, and were higher than other three groups respectively. COX regression analysis revealed that the independent predictors effecting the mortality rate included age [=0.000, OR=1.375, 95%CI(1.155, 1.637)], blood urea at admission [=0.000, OR=1.375, 95%CI(1.155, 1.637)], and blood creatinine at admission[=0.037, OR=1.213, 95%CI(1.121, 1.484)].

CONCLUSIONSElderly hip fracture patients with high serum urea and high serum creatinine at admission indicate higher fatality rate. Age, serum urea and serum creatinine at admission were independent predictors of fatality rate of elderly hip fracture patients.

OBJECTIVETo study the expression of hypoxia inducible factor 1α(HIF-1α) of iron-overloaded in irradiated mice and its effect on erythropoiesis.

METHODSTwenty mice were randomly divided into 4 groups: Ctrl (control group), IR (irradiation group), IO (irradiation + iron overload group), and RAPA (rapamycin treatment group). The iron overload model was verified. The CFU-E (colony forming unit-erythroid) and BFU-E(burst colony forming unit-erythroid) were cultured; flow cytometry was used to detect the ratios of early stage (Ter119CD71) to late stage (Ter119CD71) of primitive erythroblasts; RT-PCR was used to detect the mRNA expression of HIF-1α and its related signal molecules in bone marrow cells.

RESULTSThe expression of HIF-1α in IR and IO group was significantly higher than that in Ctrl group, and that in IO group was significantly higher than IR group (P<0.05). The ratio of late stage primitive erythroblasts, the number of CFU-E and BFU-E in both IR and IO group were lower than those in Ctrl group, and those in IO group were significantly lower than those in IR group (P<0.05). Compared with Ctrl group, the expression of HIF-1α related signal pathway molecules in both IR and IO group was significantly decreased (P<0.05). Compared with IO group, the expression of HIF-1α and its related signal molecules in RAPA(mTOR inhibitor) group was decreased significantly (P<0.05), the number of BFU-E was increased significantly(P<0.05).

CONCLUSIONIrradiation induces the increase of HIF-1α and the decrease of the ability of hematopoietic colony formation and the ratio of late stage primitive erythroblasts. Iron overload can aggravate the injury. mTOR inhibitor rapamycin can partially alleviate the injury, suggesting that iron overload can lead to injury of erythropoiesis through HIF-1α.

OBJECTIVETo assess the effect of choline in ameliorating lipopolysaccharide (LPS)-induced central nervous system inflammation and cognitive deficits in mice and explore the underlying mechanism.

METHODSSeventy-two mice were randomized into saline control group, LPS group, choline intervention group and choline control group. In the latter two groups, the mice received pretreatment with intraperitoneal injections of choline (40 mg/kg, 3 times daily for 3 consecutive days) prior to microinjection of LPS into the lateral cerebral ventricle to induce central nervous system inflammation; in saline and LPS groups, the mice were pretreated with saline in the same manner before intraventicular injection of artificial cerebrospinal fluid. Choline treatment was administered in the mice till the end of the experiment. The locomotor activity and spatial learning and memory capacity of the mice were examined. The expressions of Iba1 protein and proinflammatory cytokines (TNF-α and IL-β) I the hippocampal dentate gyrus, and the expressions of α 7nAchR, p38 MAPK and phosphorylated p38 MAPK in the hippocampus of the mice were detected.

RESULTSWater maze test showed that compared with the saline control group, the mice in LPS group exhibited significantly reduced platform crossings (P<0.05), which was significantly increased by choline pretreatment (P<0.05). The mice pretreated with LPS expressed obviously increased levels of IBA-1 protein, TNF-α, and IL-1β in the hippocampus (P<0.01), and choline pretreatment significantly lowered the expressions of IBA-1 protein and IL-1β (P<0.05). The phosphorylation level of p38 MAPK increased significantly after LPS pretreatment (P<0.05), and was reduced by choline pretreatment (P<0.05); α 7nAchR expression increased significantly in choline intervention group as compared with that in the other 3 groups (P<0.05).

CONCLUSIONCholine can probably antagonize LPS-induced hippocampal p38 MAPK phosphorylation in mice via the α 7nAchR signaling pathway to protective against LPS-induced neuroinflammation and cognitive impairment in mice.

OBJECTIVETo explore the association between body mass index (BMI) and all-cause mortality among the elderly in Beijing.

METHODSThis analysis was based on the Beijing multidimensional longitudinal study of aging (BLSA), which included 2,090 subjects over 55 years old and was followed-up from 1992 to 2012. BMI-mortality curves were drawn to find the optimal BMI range with the lowest mortality. Cox proportional hazard models were used to obtain the hazard ratios (HRs) for BMI and BMI changes in the overall population and in specific stratified populations.

RESULTSDuring follow-up, 1,164 deaths were recorded; BMI-mortality curve was U-shaped, with the lowest mortality at a BMI of approximately 25 kg/m2. After adjusting for gender, age, smoking, drinking and some pre-existing diseases, HRs for underweight, overweight and obesity compared with normal weight were 1.372 (95% CI: 1.154-1.631), 0.767 (95% CI: 0.666-0.884) and 0.871 (95% CI: 0.830-1.246), respectively. HR for BMI drop was 3.245 (95% CI: 0.824-12.772) in the underweight group and 1.892 (95% CI: 0.830-1.246) in the normal weight group, HR for BMI rise was 1.795 (95% CI: 1.243-2.591) in normal weight group and 1.962 (95% CI: 1.202-3.203) in the overweight group.

CONCLUSIONKeeping BMI in an overweight status and stable is related to a reduced mortality.

Aged ; Aged, 80 and over ; Beijing ; Body Mass Index ; Chronic Disease ; mortality ; Cohort Studies ; Female ; Humans ; Male ; Middle Aged ; Proportional Hazards Models ; Risk Factors

PURPOSE: To investigate the prevalence of spina bifida occulta (SBO) and its relationship with the presence of overactive bladder (OAB) in middle-aged and elderly people in China. METHODS: A cross-sectional community-based survey was carried out at 7 communities in Zhengzhou City, China from December 15, 2013 to June 10, 2014, where residents aged over 40 years were randomly selected to participate. All of the participants underwent lumbosacral radiographic analysis and relevant laboratory tests. A questionnaire including basic information, past medical history and present illness, and the OAB symptom score was filled out by all participants. Chi-square tests and logistic regression were used for data analysis with a P-value of <0.05 denoting statistical significance. RESULTS: A total of 1,061 subjects were qualified for the final statistical analysis (58.8±11.7 years; male, 471 [44.4%]; female, 590 [55.6%]). The overall prevalence of SBO was 15.1% (160 of 1,061): 18.3% (86 of 471) in men and 12.5% (74 of 590) in women. Among these subjects, 13.7% (145 of 1,061) had OAB: 13.2% (62 of 471) in men and 14.1% (83 of 590) in women. The results of logistic regression showed that age, SBO, history of cerebral infarction (HCI), and constipation were risk factors for OAB (P<0.05), while sex, history of childhood enuresis (HCE), body mass index (BMI), and diabetes mellitus (DM) were not (P>0.05). In men, age, SBO, and constipation were risk factors for OAB (P<0.05), while HCE, BMI, DM, HCI, and benign prostate hyperplasia were not (P>0.05). In women, age, SBO, and HCI were risk factors for OAB (P<0.05), while HCE, BMI, DM, vaginal delivery, and constipation were not (P>0.05). CONCLUSIONS: The prevalence of SBO is high and it is related to OAB in middle-aged and elderly people in China.
Aged* ; Asian Continental Ancestry Group* ; Body Mass Index ; Cerebral Infarction ; China ; Constipation ; Diabetes Mellitus ; Enuresis ; Female ; Humans ; Hyperplasia ; Logistic Models ; Male ; Prevalence* ; Prostate ; Risk Factors ; Spina Bifida Occulta* ; Spinal Dysraphism* ; Statistics as Topic ; Urinary Bladder, Overactive*

OBJECTIVETo investigate the effects of iron overload on apoptosis and function of splenic CD8+ T cells in mice.

METHODSForty C57BL/6 mice were randomly divided into control groups, Iron overload (IO), IO+NAC and IO+DFX groups. The iron overload model was established by intraperitoneal injection of iron dextran, and saline was injected as the control. The levels of intracellular reactive oxygen species (ROS) and labile iron pool (LIP) were analyzed by measuring the mean fluorescence intensity (MFI) of 2-7 dichlorofluorescein (DCF) or calcein. The ratio of CD8+ T cells and the levels of IFN-γ, TNF-α, Granzyme-B, and perforin in CD8+ T cells were detected by flow cytometry. The CD8+ T cell apoptosis was determined by flow cytometry with Annexin V/PI double staining. Real-time PCR was used to detect the expression of IFN-γ, TNF-α, Granzyme-B, perforin, BCL-2, and bax at mRNA level in CD8+ T cells.

RESULTSIron overload was found by spleen iron staining and flow cytometry. The level of intracellular ROS in iron overload (IO) groups was higher than that of the control groups (P<0.01). The percentage of CD8+ T cells in spleen from mice with IO was lower than that in control groups (P<0.05). The expression of IFN-γ and Granzyme-B in CD8+ T cells in IO group were lower than that in control group, the expression of IFN-γ and Granzyme-B at mRNA level in CD8+ T cells was lower than that of control group (P<0.05). CD8+ T cell apoptosis in iron overload group was significantly higher than that in control groups (P<0.01); the expression of BCL-2 at mRNA level was lower than that in control group, but the expression of BAX at mRNA level was higher than that in control group (P<0.05). These effects could be reversed after treating iron-overloaded mice with DFX or NAC.

CONCLUSIONIron overload can inhibit the ratio of CD8+ T cells of splenic cells in mice, decrease the expression of IFN-γ, Granzyme-B, increase the apoptosis of CD3+ CD8+/CD8-. These effects may be regulated through increasing the intracellular ROS level, and can be partially reversed after treating iron-overloaded mice with DFX or NAC.

Animals ; Apoptosis ; CD8-Positive T-Lymphocytes ; cytology ; pathology ; Granzymes ; metabolism ; Interferon-gamma ; metabolism ; Iron ; metabolism ; Iron Overload ; physiopathology ; Mice ; Mice, Inbred C57BL ; Perforin ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Random Allocation ; Reactive Oxygen Species ; metabolism ; Spleen ; cytology ; Tumor Necrosis Factor-alpha ; metabolism ; bcl-2-Associated X Protein ; metabolism

OBJECTIVETo explore the autophagy activity of CD34+ cells in bone marrow of MDS patients and its clinical significance.

METHODSThe activity of autophagy in bone marrow CD34+ cells from 20 MDS patients, 20 non-malignant anemia patients and 5 AML patients admitted in our hospital from October 2012 to March 2014 was detected by flow cytometry (FCM).

RESULTSThe autophagy activity in low risk MDS patients and non-malignant anemia patients were both significantly higher than that in both high risk MDS and AML patients (P<0.05), and more interestingly, the autophagy activity in MDS negatively correlated with World Health Organization classification-based prognostic system (WPSS) score (r=-0.877) .

CONCLUSIONThe autophagy activity CD34+ cells in the patients with MDS is higher than that in AML patients, and negatively correlated with WPSS scores, indicating that the decrease of autophagy activity maybe accelerate the genesis and development of MDS and relate with the prognosis of MDS patients.

Antigens, CD34 ; metabolism ; Autophagy ; Bone Marrow Cells ; cytology ; pathology ; Flow Cytometry ; Humans ; Leukemia, Myeloid, Acute ; pathology ; Myelodysplastic Syndromes ; pathology ; Prognosis

OBJECTIVETo compare the clinical features of children with different clinical forms of congenital hepatic fibrosis (CHF), and provides a description of the characteristics of childhood CHF.

METHODSSixty children with CHF between January 2002 and June 2015 were enrolled, including 26 children with portal hypertensive CHF (PH CHF), 3 children with cholangitic CHF, 30 children with combined portal hypertensive and cholangitic CHF (mixed CHF), and 1 child with latent forms of CHF. The medical data of 26 children with PH CHF and 30 children with mixed CHF, including gender, age, clinical manifestations, physical signs, laboratory tests and imaging characteristics, were retrospectively studied.

RESULTSFever, jaundice and hepatomegaly were more frequently noted in children with mixed CHF than in those with PH CHF (P<0.05). Splenomegaly and liver cirrhosis occurred more often in children with CHF, but there was no significant difference in the incidences of splenomegaly and liver cirrhosis between the children with PH CHF and mixed CHF. The plasma prothrombin activity, white blood cell counts, platelet counts, mean platelet volume, serum levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyl transferase, leucine aminopeptidase, and total bile acids in children with mixed CHF were higher than in those with PH CHF (P<0.05). The decreased international normalized ratio and lower serum albumin levels were more frequently observed in children with mixed CHF than in those with PH CHF (P<0.05).

CONCLUSIONSPH and mixed CHF are common forms in childhood CHF. The children with the two forms of PH usually manifest portal hypertension such as cirrhosis and hepatosplenomegaly. The liver damage may be common in children with mixed CHF.

Adolescent ; Alkaline Phosphatase ; blood ; Child ; Female ; Genetic Diseases, Inborn ; complications ; diagnosis ; Humans ; Liver Cirrhosis ; complications ; diagnosis ; Male ; Splenomegaly ; etiology